Barral J, Galarraga E, Bargas J
Neurociencias, ENEP Iztacala, UNAM, México City, México.
Brain Res Bull. 1999 Jul 1;49(4):285-9. doi: 10.1016/s0361-9230(99)00061-1.
Cholinergic presynaptic inhibition was investigated on neostriatal glutamatergic transmission. Paired pulse facilitation (PPF) of orthodromic population spikes (PS) were used to construct a concentration-response relationship for muscarine on presynaptic inhibition. Muscarine had an effect proportional to its extracellular concentration with an EC50 (mean +/- standard estimation error) of: 2.5 +/- 1.5 nM, and a maximal effect (saturation) of 245 +/- 16%. Several peptidic toxins against some voltage-gated Ca2+-channels increased PPF indicating that the Ca2+-channels they block participate in transmitter release. However, neither 1 microM omega-conotoxin GVIA, a specific blocker of N-type Ca2+-channels, nor 10-30 nM omega-agatoxinTK, a selective blocker of P-type Ca2+-channels, were able to occlude muscarine's effect on presynaptic inhibition. Nevertheless, 100-400 nM omega-agatoxinTK occluded muscarine's action on PPF in a dose-dependent manner. These results are consistent with Q-type Ca2+-channels mediating muscarinic presynaptic inhibition of neostriatal afferents.
研究了胆碱能突触前抑制对新纹状体谷氨酸能传递的影响。采用顺向群体峰电位（PS）的双脉冲易化（PPF）来构建毒蕈碱对突触前抑制的浓度-反应关系。毒蕈碱的作用与其细胞外浓度成正比，其半数有效浓度（EC50，平均值±标准估计误差）为：2.5±1.5 nM，最大效应（饱和）为245±16%。几种针对某些电压门控Ca2+通道的肽类毒素增加了PPF，表明它们所阻断的Ca2+通道参与递质释放。然而，1 μM的ω-芋螺毒素GVIA（一种N型Ca2+通道的特异性阻断剂）和10 - 30 nM的ω-阿加毒素TK（一种P型Ca2+通道的选择性阻断剂）均不能消除毒蕈碱对突触前抑制的作用。尽管如此，100 - 400 nM的ω-阿加毒素TK能以剂量依赖的方式消除毒蕈碱对PPF的作用。这些结果与Q型Ca2+通道介导新纹状体传入纤维的毒蕈碱能突触前抑制作用一致。
